SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
We describe an apparent outbreak of respiratory infection with Acinetobacter species involving 14 patients over 8 days. Epidemiological investigation revealed two consecutive pseudo-outbreaks of infection caused by two consecutive, unrelated laboratory errors in the processing of sputum, nasopharyngeal, and endotracheal aspirates.
We prospectively studied the value of systematic rectal swabs performed for the detection of colonization and the prediction of infections by Acinetobacter baumanii in 751 consecutive patients admitted to five intensive-care units (ICUs) over an 8-month period. Gastrointestinal tract colonization was found in 8.7% of ICU admissions. The positive and negative predictive values of rectal swabs for the detection of subsequent infection were 17% and 99%, respectively. Sensitivity and specificity were 55% and 93%, respectively. We also determined the comparative values of rectal or nasal swabs and skin cultures for the detection of A baumanii colonization in 25 patients already colonized or infected with A baumanii. The combination of rectal and nasal swabs was positive in 20 (80%) of 25. The results of the present study suggest that detection of gastrointestinal tract A baumanii colonization is not an accurate predictor of subsequent A baumanii infection and that combined rectal and nasal swabs might be used for the detection of A baumanii colonization in ICU patients.
Integrons from a clinical strain of Acinetobacter baumannii highly resistant to beta-lactams have been analyzed. The largest (2.2 kb) contained three gene cassettes: an aacA4, an open reading frame of 417 nucleotides, and an OXA-type encoding gene. The oxa gene nucleotide sequence differed from that of the oxa-20 in 2 bp, one of the mutations being silent. The nonsilent mutationgenerated a substitution of glutamic acid for aspartic acid. The new OXA has been named OXA-37.
BACKGROUND: Acinetobacter baumannii is a gram-negative coccobacillus that causes outbreaks of nosocomial infections in ICUs. Due to resistance to multiple antibiotics, management of clusters of A. baumannii is useful as a model in eradication of multi-drug resistant infections. We outline the evolution of an A. baumannii outbreak, focusing on methods of transmission and multidisciplinary measures aimed at eliminating it from the ICU. METHODS: Patients in an urban, tertiary care medical center from November 1996 to December 1997 having positive cultures for multi-drug resistant A. baumannii are included in this study. A. baumannii was isolated on blood agar and MacConkey cultures and identified by Vitek panel. Disk diffusion including amikacin, imipenem, polymyxin B, and sulbactam were used to determine resistance. RESULTS: An outbreak of 52 patients (27 infected, 25 colonized) with 68 positive sites began with the transfer of a colonized >50% total body surface area burn patient from an outside hospital. Within 3 days, the index patient was in the burn ICU, coronary care unit, and medical ICU. Soon, clusters of patients with A. baumannii infections sensitive only to polymyxin B were seen in those units and, ultimately, the surgical ICU. On typing, 2 strains were found, PFGE B and C. Given the level of antibiotic resistance, patients with colonization or infection were cohorted and placed on contact isolation. Strict antiseptic measures, such as hand-washing, barrier isolation, equipment and room cleaning, sterilization of ventilator equipment, and dedication of medical equipment to each patient were instituted. Still, positive environmental cultures were found in ventilator water traps, sinks, and bedrails. Sporadic cases continued for a total of 13 months, with 10 deaths resulting from the infections. CONCLUSION: A. baumannii is a mildly virulent organism that becomes resistant to antimicrobials. Because of multiple antibiotic resistance, strict contact isolation cohorting and antiseptic technique are the primary modes of containment. This outbreak serves as a model of eradication of multi-drug resistant organisms from ICUs. These measures will become of greater importance as nosocomial organisms develop increasing resistance to antimicrobials.
Between 1998 and 2000, we characterized 91 nosocomial isolates of Acinetobacter baumannii by antibiotyping and genotyping. A total of 25 ribotypes were obtained among these 91 isolates. When the isolates from surgical intensive care units (ICUs) and other wards were compared, multiresistant A. baumannii isolates with the same ribotype 25 (R-25) were significantly more prevalent in nosocomial infections among the surgical patients. Further subtyping of the strains by pulsed-field gel electrophoresis confirmed that strains of the same ribotype in surgical ICUs and a few isolates from other wards were identical or clonally related. Different antibiotic resistance profiles were observed among these R-25 isolates. All R-25 isolates contained intI1 integrase, and two clusters of integron cassettes were found. These clusters of cassettes were encoded by an open reading frame (ORF) of -5'CS-aac(3)Ia-aadA1a-unknown or f-3'CS or 5'CS-aacA4-aadA1-catB8-3'CS, indicating the involvement of different resistant genes. Two isolates contained bla (IMP-1), which was acquired from a conjugatively transferable plasmid and did not involve integron-associated resistance. In conclusion, an epidemic of nosocomial infections associated with A. baumannii strains that have different resistance profiles was identified. Resistance profiles can change by a combination of plasmid- and integron-associated acquisition, especially in a unit with high antibiotic selective pressures. Infectious control personnel should be alert to the change in resistance profiles during routine monitoring.
We report our experience with two cases of fixation device-related orthopedic infections due to multidrug-resistant Acinetobacter baumannii strains. Both patients were successfully treated with intravenous administration of colistin, despite the reported poor penetration of this medication to these tissues, in the old literature. No serious colistin-associated toxicity developed and no recurrence of the infection occurred on follow up.
To identify risk factors for and prognostic indicators of the nosocomial acquisition of multiresistant Acinetobacter baumannii in an intensive care unit, we prospectively studied 40 patients: 13 who were infected with this organism and 27 who were colonized. Isolates were identified by pulsed-field gel electrophoresis; the infected/colonized patients were compared with 348 noninfected, noncolonized patients by logistic regression analysis and with matched historical controls in a cohort study. The severity of illness (evaluated by the APACHE II score; P < .05) and previous infection (P < .001) were retained as independent risk factors for acquiring A. baumannii. Logistic regression analysis selected a high APACHE II score (P < .01) and the acquisition of A. baumannii (P < .01) as factors independently associated with death. The acquisition of A. baumannii was associated not only with high mortality but also with a length of stay on the intensive care unit in excess of that due to the underlying disease alone; specifically, the attributable mortality was 25%, with a risk ratio for death of 2.0 (95% confidence interval, 1.11-3.62), and the duration of stay for infected/colonized patients was 10.3 days longer than that for controls (P < .001).
The number of nosocomial infections caused by Acinetobacter baumannii has increased in recent years. During a 12-month study, there were 1.8 episodes of A. Baumannii bacteremia per 1,000 adults admitted to a hospital in Seville, Spain. Seventy-nine patients were included in the study. A. baumannii bacteremia occurred after a mean (+/- SD) hospitalization of 18 +/- 20 days. In all cases the infections were acquired nosocomially; 71% wee acquired in intensive care units. Ampicillin/ sulbactam was found to be the most active agent against A. baumannii. The common source of the bacteremia was the respiratory tract (32 cases [71%]). Twenty patients (25%) had septic shock, and 24 (30%) had disseminated intravascular coagulation (DIC). Treatment with imipenem or ampicillin/sulbactam was most effective (cure rates, 87.5% and 83%, respectively). The deaths of 27 patients (34%) were related to A baumannii bacteremia. The presence of DIC (odds ratio [OR] = 116.4; P < .0001) and inappropriate antimicrobial treatment (OR = 15.2; P < .01) were independently associated with mortality. We conclude that most A. baumannii isolates are multiresistant and that nosocomial A. baumannii bacteremia may cause severe clinical disease that is associated with a high mortality.
Fecal colonization with multiresistant Acinetobacter baumannii was evaluated in 189 consecutive patients in intensive care units (ICUs) during two different 2-month periods (October-November 1993 and May-June 1994). Rectal swabs were obtained weekly from admission to discharge from the ICU. Overall, 77 patients (41%) had multiresistant A. baumannii fecal colonization; colonization was detected in 55 (71%) of the patients within the first week of their ICU stay. Clinical infections due to multiresistant A. baumannii occurred more frequently in patients with fecal colonization than in those without fecal colonization (26% vs. 5%, respectively; P < .001). The reinforcement of isolation measures between study periods reduced both the number of fecal carriers of multiresistant A. baumannii (from 52% to 31%; P < .01) and the number of patients with multiresistant A. baumannii infections (from 17% to 11%; no statistical significance). The digestive tract of ICU patients could be an important epidemiologic reservoir for multiresistant A. baumannii infections in hospital outbreaks. Further prospective studies should be undertaken to define the relative significance of digestive tract colonization compared with other body site colonizations.
We evaluated the spread of Acinetobacter baumannii strains among three hospitals located in São Paulo, Brazil. A total of 46 isolates, which were typed by chromosomal DNA analysis with use of pulsed field gel electrophoresis (PFGE), were tested for susceptibility to the fluoroquinolones, carbapenems, aminoglycosides (amikacin), cephalosporins, polymyxin B, and ampicillin/sulbactam by means of the broth microdilution method, disk diffusion, and the E-test. Isolates with an identical PFGE pattern (pattern B) that were susceptible only to carbapenems, polymyxin B, and ampicillin/ sulbactam were recovered in all three hospitals. In addition, isolates with PFGE pattern A that were susceptible only to polymyxin B and ampicillin/sulbactam were recovered in hospitals 1 and 2. The results of our study strongly suggest the interhospital transmission of multiresistant epidemic strains of A. baumannii in São Paulo. Once in the hospital, these strains can disseminate and cause outbreaks with devastating consequences.
The clinical features and the outcomes of eight cases of nosocomial Acinetobacter baumannii meningitis treated with ampicillin/sulbactam are reported. All the patients had fever, neck stiffness or meningeal signs, and a low consciousness level, and in their cerebrospinal fluid (CSF), pleocytosis, a low glucose level, and an elevated protein level were noted. For all CSF isolates of A. baumannii, the MIC of ampicillin/sulbactam was < or = 8/4 microg/mL. The MICs of sulbactam by microdilution in two cases were 4 microg/mL. All isolates were resistant to cefotaxime, ceftriaxone, ceftazidime, ureidopenicillins, ciprofloxacin, and gentamicin. Seven isolates were resistant to imipenem. A. baumannii was isolated from other samples in seven episodes. All patients were treated with ampicillin/sulbactam (seven with 2 g/l g every 6 hours and one with 2 g/l g every 8 hours). Six patients were cured and two patients died of meningitis. There were no side effects with the ampicillin/sulbactam treatment. In conclusion, ampicillin/sulbactam may be effective as therapy for meningitis caused by A. baumanii resistant to imipenem and other beta-lactam drugs.
The virulence of clinical isolates of Acinetobacter calcoaceticus subsp. anitratus was studied in mice, and in-vitro and in-vivo activities of several antimicrobial agents were evaluated. In in-vitro susceptibility testings, tetracyclines, aminoglycosides, and peptide were highly sensitive, and minocycline and doxycycline were the most active of 21 antibiotics tested against 84 clinical isolates of Acin. calcoaceticus. Virulence tests for mice revealed that some strains exhibited high virulence with LD50 values between 10(3) and 10(4) viable cells/mouse. Against lethal and urinary tract infections produced by Acin. calcoaceticus Ac-54 strain in mice, minocycline, doxycycline, gentamicin, and dibekacin, which were highly active in vitro, were effective.
The antibacterial activities of sulbactam and YTR830H, both beta-lactamase inhibitors, were studied against Acinetobacter calcoaceticus, in vitro and in vivo. In-vitro susceptibility tests showed both to be very active against 80 clinical isolates of A. calcoaceticus. Against an intraperitioneal infection in mice, caused by A. calcoaceticus Ac54, the 50% effective doses of sulbactam and YTR830H were 1.62 and 16.7 mg/kg, respectively. Against A. calcoaceticus S31, a strain resistant to gentamicin, sulbactam and YTR830H were active both in vitro and in vivo.
From March 1995 to March 1997, sulbactam was prospectively evaluated in patients with non-life-threatening multiresistant Acinetobacter baumannii infections. During this period, 47 patients were treated with sulbactam; of them, five were excluded because they had received < or =48 h of sulbactam therapy. A total of 42 patients, 27 males and 15 females with a mean age of 60+/-15 years, were finally evaluated. Infections were as follows: surgical wound, 19; tracheobronchitis, 12; urinary tract, 7; catheter-related bacteraemia, 2; and pneumonia, 2. Eighteen patients received intravenous sulbactam alone (1 g every 8 h) and 24 patients received intravenous sulbactam/ampicillin (1 g:2 g every 8 h) with no major adverse effects. Of the 42 patients, 39 improved or were cured and showed A. baumannii eradication and one patient had persistence of wound infection after 8 days of sulbactam/ampicillin requiring surgical debridement. Two patients died after 3 days of therapy (one of the deaths was attributable to A. baumannii infection). The in-vitro activity of the sulbactam/ampicillin combination was by virtue of the antimicrobial activity exhibited by sulbactam. Killing curves showed that sulbactam was bacteriostatic; no synergy was observed between ampicillin and sulbactam. Our results indicate that sulbactam may prove effective for non-life-threatening A. baumannii infections. Its role in the treatment of severe infections is unknown. However, the current formulation of sulbactam alone may allow its use at higher doses and provide new potential synergic combinations, particularly for those infections by A. baumannii resistant to imipenem.
Acinetobacter baumannii is a common cause of nosocomial pneumonia and other nosocomial infections. Multiresistant A. baumannii has also a high prevalence, which can make effective treatment difficult. We designed a new model of A. baumannii experimental pneumonia using C57BL/6 immunocompetent mice. This model was used to compare the efficacy of imipenem, doxycycline and amikacin in monotherapy, and the combination of imipenem plus amikacin and doxycycline plus amikacin. Doxycycline plus amikacin were synergic in vitro after 24 h incubation, whereas imipenem plus amikacin showed no in vitro synergy. The number of sterile lungs and the lung clearance of A. baumannii were greater in the group treated with imipenem than in those treated with amikacin or doxycycline in monotherapy (P < 0.05). The combination of imipenem plus amikacin and doxycycline plus amikacin was no more effective than imipenem alone in the clearance of organisms from lungs (2.42 +/- 1.46 cfu/g versus 2.7 +/- 1.5 cfu/g versus 1.23 +/- 1.02 cfu/g). These results suggest that the addition of amikacin does not improve the results obtained by imipenem monotherapy. Doxycycline plus amikacin is an alternative to imipenem in the therapy of A. baumannii pneumonia.
Sulbactam and imipenem were compared in an experimental pneumonia model in immunocompetent mice, using a susceptible strain of Acinetobacter baumannii, and in an experimental endocarditis model in rabbits, using an intermediately susceptible strain. In the former, sulbactam was as efficacious as imipenem in terms of survival, sterility of lungs and in the bacterial clearance from lungs and blood, provided that the t > MIC for sulbactam (1.84 h) was similar to that for imipenem (2.01 h). In the endocarditis model, imipenem (t > MIC, 2.12 h) was more efficacious than sulbactam (t > MIC, 1.17 h) in bacterial clearance from vegetations. These results show the efficacy of sulbactam in infections caused by susceptible strains of A. baumannii, with an MIC up to 4 mg/L, provided that doses reach a t > MIC similar to that of imipenem. The activity of sulbactam was time dependent.
The effect of a selective decontamination of the digestive tract (SDD) regimen including polymyxin and tobramycin on several body site reservoirs was compared between a test group and a control group in intensive care unit (ICU) patients with faecal multi-resistant Acinetobacter baumannii colonization. SDD significantly reduced faecal and pharyngeal carriage when compared with the control group at the end of ICU stay (48% versus 91%, P = 0.001, and 38.5% versus 78%, P = 0.01, respectively), but failed to reduce axillary colonization (75% versus 78%, P = 0.6). In addition, the isolation of A. baumannii from new clinical samples was lower in patients with SDD (45.5% versus 81%, P = 0.05). No resistance to polymyxin was observed. We conclude that the digestive tract reservoir of A. baumannii in ICU patients may be decreased by a SDD regimen.
The in vitro activity of clinafloxacin was studied in comparison with ciprofloxacin, levofloxacin, moxifloxacin, nalidixic acid, sparfloxacin and trovafloxacin against Acinetobacter baumannii clinical isolates. Clinafloxacin showed a MIC(90) of 4 mg/L, whereas the remaining quinolones showed a MIC(90) equal to or higher than 16 mg/L. MIC(50) determination in the presence of reserpine resulted in a two-fold decrease, except for trovafloxacin, which decreased four-fold, and for moxifloxacin and nalidixic acid, which did not change. The effect of reserpine was most pronounced among strains with a low level of resistance to quinolones. The MIC of clinafloxacin for strains with no mutation in either gyrA or parC genes ranged from 0.008 to 0.25 mg/L. In strains with a single mutation at amino acid codon Ser83 of the gyrA gene, the MIC of clinafloxacin ranged from 0.12 to 1 mg/L, whereas strains with a double mutation, one in the gyrA gene and another in the parC gene, showed a range of MIC of clinafloxacin from 1 to 8 mg/L. Therefore, clinafloxacin shows good activity against strains carrying a single mutation in the gyrA gene, and hence a second mutation is required for the microorganism to express resistance.